Effects of a mindfulness-based interventions on stress, burnout in nurses: a systematic review and meta-analysis.

Background: Stress in the healthcare environment causes negative effects in nurses such as burnout, anxiety, and depression. The COVID-19 pandemic has resulted in increased pressure on medical staff globally, highlighting the potential benefits of mindfulness-based interventions in reducing nurses' stress levels. Despite numerous studies exploring the effect of mindfulness-based training on nurses, the results remain inconclusive. Objective: To systematically evaluate the impact of mindfulness training on nurse's performance and increase the certainty of existing evidence. Methods: This study searched various databases, including EBSCO, Embase, Web of Science, PubMed, ProQuest, Scopus, Cochrane Online Library, Wanfang, SinoMed, CNKI, and VIP, for randomized controlled trials on the impact of mindfulness-based interventions for nurses up until 02 December 2022. Two investigators independently screened and extracted data from the articles, while also assessing the risk of bias. The data was analyzed using RevMan 5.4 software. Results: This review identified 15 studies out of the 2,171 records retrieved, consisting of a total of 1,165 participants who were randomized. Post-intervention analysis provided very-low certainty evidence of moderate effectiveness of mindfulness-based training in reducing stress [standardized mean difference (SMD) = -0.81; 95% confidence interval (CI) = -1.11 to -0.52], with no significant effect on anxiety (SMD = -0.30; 95% CI = -0.72 to 0.13) or depression (SMD = -0.24; 95% CI = -0.55 to 0.07). However, the training was effective in reducing burnout, as demonstrated by the lower scores for emotional exhaustion (SMD = -4.27; 95% CI = -5.94 to -2.59) and depersonalization (SMD = -2.89; 95% CI = -4.24 to -1.54) and higher scores for personal accomplishment (SMD = 2.81; 95% CI = 0.12 to 5.50). There was a sustained improvement in stress levels in the short-term (≤3 months), with delayed benefits for burnout. However, only two studies were available for later follow-ups, and there was no significant evidence of long-term effects. Conclusion: Mindfulness-based training may be a viable intervention for improving the psychological wellbeing of nurses, including reducing stress, burnout. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42023387081.

Protective effect of citicoline on random flap survival in a rat mode.

BACKGROUND: Medical therapy for flap survival has been extensively investigated. In this study, we explored the effect of citicoline (CDP-choline, CDPC), used for clinical treatment of cerebral trauma, on random skin flap survival in rats. MATERIALS AND METHODS: Sixty rats were divided into three groups: low-dose (CDPC-L), high-dose (CDPC-H), and control. The CDPC-L and CDPC-H groups were intraperitoneally injected with 100 mg/kg and 300 mg/kg CDPC every day, respectively; the control group was injected with an equivalent volume of normal saline. The survival region was assessed on the 7th day after the flap operation. The microvascular density and neutrophil density were measured by hematoxylin and eosin staining. Lead angiography was used to detect angiogenesis, and laser Doppler was used to detect blood perfusion. Expression levels of vascular endothelial growth factor (VEGF), interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, Toll-like receptor (TLR) 4, and nuclear factor kappa B (NF-κB) were detected by immunohistochemistry. Malondialdehyde and superoxide dismutase were used to determine the lipid peroxidation level. RESULTS: The average survival region of the flap was significantly larger in the CDPC-H group than in CDPC-L and control groups, with less ischemic necrosis. VEGF expression, microvascular density, angiogenesis, blood perfusion, and superoxide dismutase in the flap were higher in the CDPC-H group than in the CDPC-L and control groups. In addition, levels of neutrophil density, IL-1ß, IL-6, TNF-α, TLR4, NF-κB, and malondialdehyde decreased significantly in the CDPC-H group. CONCLUSION: High-dose CDPC injection after a random flap operation is beneficial for flap survival.

Resveratrol attenuates adenosine diphosphate-induced platelet activation by reducing protein kinase C activity.

Inappropriate platelet activation is the key point of thrombogenesis. The aim of the present study was to investigate the effects of resveratrol (RESV), a compound extracted from the Chinese medicinal herb Polygonum cuspidatum sieb et Zucc, on the platelet activation induced by adenosine diphosphate (ADP) and its possible mechanism. The percentage of platelet aggregation and surface P-selectin-positive platelets, and the activity of protein kinase C (PKC) of platelet were observed with platelet aggregometer, flow cytometry and phosphorimaging system, respectively. RESV at 25, 50 and 100 microM showed anti-platelet aggregation and inhibition of surface P-selectin-positive platelets in a concentration-dependent manner. RESV (50 microM) inhibited the activity of PKC in the membrane fraction of platelets and decreased the percentage of membrane associated PKC activity in total PKC activity. Moreover, DL-erythro-1,3-Dihydroxy-2-aminooctadecane, an elective protein kinase C inhibitor (PKCI), and RESV had additive effects of inhibiting the percentage of platelet aggregation and surface P-selectin-positive platelets. It is suggested that RESV may inhibit platelet aggregation, the percentage of surface P-selectin-positive platelets and subsequent thrombus formation. The mechanisms may be partly relative to the decrease of the activity of PKC of platelets.

[Inhibitory effects of emodin on proliferation of rat vascular smooth muscle cell induced by angiotensin II].

OBJECTIVE: To investigate the effects of emodin on the proliferation of cultured rat vascular smooth muscle cell (VSMC) induced by angiotensin II. METHOD: VSMCs were cultured by explant method. Cell proliferation model was established by stimulation with Ang II. Cell proliferation was measured by MTT assay to observe the effects of emodin (10, 20, 40 and 80 micromol x L(-1)) and N(G)-nitro-L-arginine methyl ester (L-NAME, 100 micromol x L(-1)) on VSMC proliferation induced by Ang II. The expression of PCNA was measured by immunohistochemical staining. Nitric oxide (NO) level was measured by Griess reagent. Nitric oxide synthase (NOS) and inducible nitric oxide synthase (iNOS) levels were detected by chemical colorimetric method. mRNA expression of iNOS was measured by reverse transcription polymerase chain reaction (RT-PCR). RESULT: Emodin at the doses range from 10 to 80 mol x L(-1) inhibited cell proliferation in a dose and time-dependent manner. The inhibitory effects were partly blocked by 100 mol x L(-1) of L-NAME. Emodin markedly decreased the expression of PCNA in VSMC, increased NO, NOS and iNOS levels, and increased iNOS mRNA expression in VSMC. CONCLUSION: Emodin could inhibite VSMCs proliferation induced by Ang II. Inhibiting the expression of PCNA, increasing the NO secretion and upregulating the iNOS gene expression might be associated with the inhibitory effects.

Inhibitory effects of emodin on the proliferation of cultured rat vascular smooth muscle cell-induced by angiotensin II.

Rhubarb, used as a traditional Chinese medicine for centuries, offers therapeutic potential for cardiovascular and other diseases. Emodin, extracted from the root extract of rhubarb has sparked increasing interest for therapeutic application. The main objective was to study the effect of emodin on cultured vascular smooth muscle cells (VSMCs) proliferation induced by angiotensin II (Ang II) and the expression of proto-oncogene c-myc. VSMCs were cultured by the explant method, then incubated for 24, 48 and 72 h with emodin (10-80 microm) and Ang II, or were left untreated (control). Cell proliferation was measured by MTT assay and immunohistochemical staining for proliferating cell nuclear antigen (PCNA), respectively. The expression of c-myc was measured by immunohistochemical staining and image analysis technique. Ang II increased the cell proliferation compared with the control group (p < 0.01). The expression of PCNA and c-myc was increased compared with the control group (p < 0.01). After pretreatment with emodin, the above indexes were obviously reduced compared with the Ang II group (p < 0.01). These findings suggested that emodin inhibited VSMCs proliferation induced by Ang II. Inhibition of the expression of c-myc might be correlated with the inhibitory effects.

Inhibition of vascular smooth muscle cell proliferation by serum from rats treated orally with Gastrodia and Uncaria decoction, a traditional Chinese formulation.

AIM: This study was to investigate the effect of serum from rats treated orally with GUD on vascular smooth muscle cells (VSMCs) proliferation in vitro. METHODS: Cell proliferation was measured by Methyl thiazolyl tetrazolium (MTT) assay. Expression of proliferating cell nuclear antigen (PCNA) and proto-oncogene c-myc were measured by immunochemical staining and image analysis. Griess reagent were used to detect nitric oxide (NO) level. Endothelin-1 (ET-1) level was measured by radioimmunoassay. RESULTS: GUD serum (2.5%-10%) inhibited VSMCs proliferation in a dose and time-dependent manner. GUD serum inhibited the expression of PCNA and c-myc. Moreover, GUD serum increased nitric oxide (NO), and decreased Endothelin-1 (ET-1) level in culture medium. CONCLUSION: GUD serum exhibited directly inhibitory effect in VSMCs proliferation. Inhibiting the expression of PCNA and c-myc, increasing NO level and decreasing ET-1 level might be associated with the antiproliferative effect.

Yangxueqingnao particles inhibit rat vascular smooth muscle cell proliferation induced by lysophosphatidic acid.

OBJECTIVE: To observe the effect of Yangxueqingnao particles on rat vascular smooth muscle cell (VSMC) proliferation induced by lysophosphatidic acid (LPA). METHODS: The amount of (3)H-TdR ((3)H-thymidine) admixed in cultured rat VSMC was measured and mitogen-activated protein kinase (MAPK) activity and lipid peroxidation end product malondialdehyde (MDA) content of the VSMC were assayed. RESULTS: 1x10(-9), 1x10(-8), 1x10(-7) mol/L LPA in a concentration dependent manner, induced the amount of (3)H-TdR admixed, MAP kinase activity, and MDA content of the cultured rat VSMC to increase. However, 5%, 10%, and 15% Yangxueqingnao serum preincubation resulted in a decrease of 23.0%, 42.0%, and 52.0% (P<0.01) respectively in the amount of (3)H-TdR admixed, a decline in VSMC MAP kinase activity of 13.9% (P<0.05), 29.6% (P<0.01), and 48.9% (P<0.01) respectively, and also, a decrease in MDA content of VSMC of 19.4%, 24.7%, and 43.2% (P<0.01) respectively, in the 1x10(-7) mol/L LPA-treated VSMC. CONCLUSIONS: LPA activates the proliferation and lipid peroxidation of VSMC in a concentration dependent manner. The LPA-induced VSMC proliferation is related to the activity of MAP kinases, enzymes involved in an intracellular signalling pathway. The results of the present study showed that Yangxueqingnao particles can effectively inhibit LPA-induced VSMC proliferation, MAP kinase activation, and reduce lipid peroxidative lesion.

[Cloning, expression and sequence analysis and tissue distribution of angiotensin-converting enzyme 2 (ACE2) gene in adult mice].

OBJECTIVE: o clone angiotensin-converting enzyme 2(ACE2) gene, to analyze its amino acids and nucleotides sequence and to investigate tissue distribution of ACE2 in adult mice. METHODS: The full-length ACE2 encoding sequence was amplified from the RNA of mice kidney tissue by RT-PCR technique, cloned into plasmid pGEM-T easy, then subcloned into plasmid pcDNA3.1+. After identification of DNA sequence, the recombinant plasmid pmACE2 was transfected into Cos7 cells with lipofectin reagent. The transient expression of ACE2 molecule was detected by SDS-PAGE. Sequence analysis was conducted with CLUSTALX program. Tissue distribution of ACE2 in mice was detected by RT-PCR. RESULTS: A fragment about 2.6 kb was amplified and the recombinant plasmid pmACE2 was confirmed by two-enzyme digesting and DNA sequencing. The cloned DNA sequence was consistent with that previously reported, except for 3 variations: A701G, T1102C and T1330C. SDS-PAGE proved that expression of a soluble, truncated products form of ACE2 was a glycoprotein of approximately 80 kD in Cos7 cells. The predicted mice ACE2 sequence contained an N-terminal signal sequence (amino acid residues 1-18), a single HHEMGHIQ zinc-binding domain (amino acid residues 373-380) and C-terminal membrane anchor (amino acid residues 738-765). Mice ACE2 showed 84 % identity with that of human, and 90 % identity with that of rat. Expression of ACE2 was the greatest in lungs, hearts and kidneys, and moderate levels were also detected in testes and livers. CONCLUSION: Mice ACE2 gene has been cloned and successfully expressed in vitro. The tissue-specific expression of ACE2 in different species is not identical.

[Effects of Ginkgo biloba extract on number and activity of endothelial progenitor cells from peripheral blood].

AIM: To investigate whether Ginkgo biloba extract can augment endothelial progenitor cell (EPC) number, and promote EPC proliferation, migration and adhesion. METHODS: Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days of culture, attached cells were stimulated with Ginkgo biloba extract (10, 25 and 50 mg x L(-1)) or vehicle control for the respective time points (6, 12, 24 and 48 h). EPC were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPC were further documented by demonstrating the expression of CD34, VEGFR-2 and AC133 with flow cytometry. EPC proliferation, migration and in vitro vasculogenesis activity were assayed with MTT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating MNCs on fibronectin-coated dishes, and then counting adherent cells. RESULTS: Incubation of isolated human MNCs with Ginkgo biloba extract increased the number of EPC, maximum at 25 mg x L(-1), 24 hours (approximately 1-fold increase, P < 0.01). In addition, Ginkgo biloba extract promotes EPC proliferative, migratory, adhesive and in vitro vasculogenesis capacity. CONCLUSION: Ginkgo biloba may promote EPC augmentation and enhance its functional activity.

[Effects of puerarin on number and activity of endothelial progenitor cells from peripheral blood].

OBJECTIVE: To investigate whether puerarin can augment endothelial progenitor cells (EPCs) numbers, promote EPC proliferation, migration and adhesion. METHOD: Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days culture, attached cells were stimulated with puerarin (to make a series of final concentrations: 0. 1, 0.5, 1, 3 mmol x L(-1)) or vehicle control for the respective time points (6, 12, 24, 48 h). EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. EPCs proliferation, migration and in vitro vasculogenesis activity were assayed with MT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating those on fibronectin-coated dishes, then adherent cells were counted. RESULT: Incubation of isolated human MNCs with puerarin dose increased the number of EPCs, maximum at 3 mmol x L(-1), 24 hours (approximately 1-fold increase, P < 0.01). In addition, puerarin also promoted EPC proliferative, migratory, adhesive and in vitro vasculogenesis capacity. CONCLUSION: Puerarin can augment the number of EPCs with enhanced functional activity.

Effects of Ginkgo biloba extract on number and activity of endothelial progenitor cells from peripheral blood.

The aim of this study is to investigate whether Ginkgo biloba extract can augment endothelial progenitor cells numbers, and promote the cells' proliferative, migratory, adhesive, and in vitro vasculogenesis capacity. Total mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days culture, attached cells were stimulated with Ginkgo biloba extract (to make a series of final concentrations: 10 mg/L, 25 mg/L, and 50 mg/L) or vehicle control for the respective time points (6 hours, 12 hours, 24 hours, and 48 h). Endothelial progenitor cells were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining under a laser scanning confocal microscope. They were further documented by demonstrating the expression of KDR, VEGFR-2, and AC133 with flow cytometry. Endothelial progenitor cells proliferation, migration, and in vitro vasculogenesis activity were assayed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, modified Boyden chamber assay, and in vitro vasculogenesis kit, respectively. Endothelial progenitor cells adhesion assay was performed by replating those on fibronectin-coated dishes, and then counting adherent cells. Incubation of isolated human mononuclear cells with Ginkgo biloba extract dose- and time-dependently increased the number of endothelial progenitor cells, maximum at 25 mg/L, 24 hours (approximately 1-fold increase, P < 0.01). In addition, Ginkgo biloba extract also dose- and time-dependently promoted endothelial progenitor cells proliferative, migratory, adhesive, and in vitro vasculogenesis capacity. The results of the present study defined a novel functional effect of Ginkgo biloba extract: the augmentation of endothelial progenitor cells with enhanced functional activity.

[Effect of puerarin on L-type calcium channel in isolated rat ventricular myocytes].

OBJECTIVE: To observe the effect of Puerarin on L-type calcium channel in isolated rat ventricular myocytes. METHOD: The cardiac ventricular myocytes were isolated enzymatically by Langendorff perfusion techniques at constant flow rate. Whole-cell recording of patch-clamp techniques was used to observe the current of L-type calcium channel. RESULT: Puerarin 2.4 mmol x L(-1) could inhibit the current of L-type calcium channel of rat ventricular myocytes and this inhibition was time-dependent. Purerarin elevated the current-voltage (I-V) curve of calcium current. CONCLUSION: Puerarin can inhibit L-type calcium current of rat ventricular myocytes. Which implies that puerarin takes part in anti-myocardial ischemia and anti-arrhythmics partly due to the inhibition of L-type calcium channel.

Salvia miltiorrhiza attenuates the changes in contraction and intracellular calcium induced by anoxia and reoxygenation in rat cardiomyocytes.

The aim of the present study is to investigate the effect of Salvia miltiorrhiza (SM) on contraction and the intracellular calcium of isolated ventricular myocytes during normoxia or anoxia and reoxygenation using a video tracking system and spectrofluorometry. Cardiac ventricular myocytes were isolated enzymatically by collagenase and exposed to 5 min of anoxia followed by 10 min of reoxygenation. SM (1-9 g/L) depressed both contraction and the [Ca(2+)](i) transient in a dose-dependent manner. SM did not affect the diastolic calcium level and the sarcolemmal Ca(2+) channel of myocytes but decreased the caffeine-induced calcium release. During anoxia, the +/-dL/dtmax, amplitudes of contraction (dL) of cell contraction and [Ca(2+)](i) transients were decreased, while the diastolic calcium level was increased. None of the parameters returned to the pre-anoxia level during reoxygenaton. However, SM (3 g/L) did attenuate the changes in cell contraction and intracellular calcium induced by anoxia and reoxygenation. It is concluded that SM has different effects on normoxic and anoxic cardiomyocytes. The SM-induced reduction of changes in contraction and intracellular calcium induced by anoxia/reoxygenation indicates that SM may be beneficial for cardiac tissue in recovery of mechanical function and intracellular calcium homeostasis.

[Effect of tetradrine on electrophysilogic changes caused by rising of left ventricular preload in guinea pigs].

OBJECTIVE: To investigate the changes of guinea pig heart electrophysiological properties caused by increasing left ventricular preload, and to assess the effects of tetradrine on these changes. METHOD: Working model preparation of guinea pig hearts in vitro was used, and the preload of left ventricle was increased by adjusting the prefusion pressure of left atria. The changes of heart electrophysiologic parameters including monophasic action potential duration (MAPD90), monophasic action potential amplitude (MAPA), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) were observed before and after altering the preload of left ventricle, and compared in the absence and presence of tetradrine, streptomycin or verapamil. RESULT: The rising of left ventricular preload led to shortening of MAPD90, ERP, and to descent of MAPA, VFT (all P<0.01). Both Tetradrine and streptomycin inhibited these changes of heart electrophysiologic parameters caused by elevation of left ventricular afterload (all P<0.01). In contrast, verapamil had no effects on the preload-related electrophysiological changes (all P>0.05). CONCLUSION: Electrophysiologic changes caused by increasing left ventricular preload may be inhibited by tetrandrine, through inhibition of stretch-activated ion channels.